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• W1972382107 abstract "The clinical manifestation and natural history of myocarditis range is variable from asymptomatic stages to intractable circulatory compromise and death. Supportive therapy is paramount in the treatment of this condition. The use of mechanical circulatory support as bridge-to-recovery or bridge-to-transplantation in cases of cardiovascular collapse is often the only therapeutic option for these patients. We report the case of an adolescent boy with toxic myocarditis, due to cannabis abuse, who was supported with a Thoratec left ventricular assist device (Thoratec Laboratories Corp, Pleasanton, CA) for 96 days before device removal. The clinical manifestation and natural history of myocarditis range is variable from asymptomatic stages to intractable circulatory compromise and death. Supportive therapy is paramount in the treatment of this condition. The use of mechanical circulatory support as bridge-to-recovery or bridge-to-transplantation in cases of cardiovascular collapse is often the only therapeutic option for these patients. We report the case of an adolescent boy with toxic myocarditis, due to cannabis abuse, who was supported with a Thoratec left ventricular assist device (Thoratec Laboratories Corp, Pleasanton, CA) for 96 days before device removal. The broad spectrum cause, clinical expression, and natural history of myocarditis, together with the difficulty in the accurate diagnostic evaluation of the disease, render this condition very challenging for the clinician. Supportive treatment with standard heart failure medicine including inotropic support and intra-aortic balloon counterpulsation, combined with hemodynamic monitoring is paramount in treating this condition. The use of mechanical circulatory support as bridge-to-recovery or bridge-to-transplantation in cases of cardiovascular collapse has emerged as a very effective treatment for these patients. We report the case of a young boy with severe heart failure secondary to a drug-induced (cannabis) myocarditis who required support by a Thoratec left ventricular assist device (LVAD) (Thoratec Laboratories Corp, Pleasanton, CA). His cardiac function fully recovered 96 days later, and the LVAD could be successfully removed. A previously healthy 16-year-old teenager (63 kg, 180 cm, body surface area 1.80 m2) was admitted to our hospital after being diagnosed with acute left heart failure due to acute myocarditis. Transesophageal echocardiography showed a severely dilated left ventricle with an ejection fraction of 15% and global hypokinesis, moderate to severe mitral regurgitation, moderate pulmonary hypertension, small pericardial effusion, and a mobile left ventricular apical thrombus. The electrocardiogram recorded showed sinus tachycardia, right axis deviation, slow R-wave progression in leads V1–4 and negative T waves in leads II, III, aVF, and V4–6. His initial blood investigation results, echocardiography measurements, and hemodynamic status are shown in Table 1. The usual screening for infectious myocarditis was negative, but the patient's urine testing for cannabinoids was positive. He was initially treated with intravenous diuretics, ACE inhibitors, and dobutamine. Despite maximal medical treatment, including levosimendan therapy, his clinical and hemodynamic status deteriorated 36 hours later with hypotension, cardiac index of 1.60 L/min/m2 and cardiogenic shock, with threatening multiple organ failure. The patient was evaluated and accepted for ventricular assist device therapy.Table 1Initial Baseline Patient Evaluation (Echocardiography, Right Heart Catheterization, Laboratory Results)Hemodynamic and Echocardiographic DataValueLaboratory DataValueLVEDd (mm)74Hb (Normal range, 13–18 g/dL)13.6LVESd (mm)68PLT (150,000–350,000/mm3)94,000LVEF (%)15CPK/CPK-MB/cTnI (CPK <171 U/l; CPK-MB <6.4 ng/ml; cTnI <0.04 ug/l)343/1/0.03Mean BP (mm Hg)72BUN/Crea (BUN < 50 mg/dL; Crea < 1.2 mg/dL)66/1.4RA (mm Hg)13SGOT (< 35 U/L)9,180Mean PA (mm Hg)34SGPT (< 45 U/L)4,840PCW (mm Hg)19CRP (< 0.5 mg/d)6.68SVR (Wood)21.45INR2.3PVR (Wood)5.45Na+ (135–145 mmol/L)135CI (L/min/m2)1.57NT-pro-BNP (< 125 pg/mL)16,160BP = blood pressure; BUN = blood urea nitrogen; CI = cardiac index; CPK = creatine kinase; crea = creatinine; CRP = C-reactive protein; cTnI = cardiac troponin I; Hb = hemoglobin; INR = international normalized ratio; LVEDd = left ventricular end-diastolic diameter; LVEF = left ventricular ejection fraction; LVESd = left ventricular end-systolic diameter; NT-pro-BNP = n-terminal pro-brain natriuretic peptide; PA = pulmonary artery; PCW = pulmonary capillary wedge; PLT = platelet count; PVR = pulmonary arteriolar resistance; RA = right atrium; SGOT = AST/aspartate aminotransferase; SGPT = ALT/alanine aminotransferase; SVR = systemic vascular resistance. Open table in a new tab BP = blood pressure; BUN = blood urea nitrogen; CI = cardiac index; CPK = creatine kinase; crea = creatinine; CRP = C-reactive protein; cTnI = cardiac troponin I; Hb = hemoglobin; INR = international normalized ratio; LVEDd = left ventricular end-diastolic diameter; LVEF = left ventricular ejection fraction; LVESd = left ventricular end-systolic diameter; NT-pro-BNP = n-terminal pro-brain natriuretic peptide; PA = pulmonary artery; PCW = pulmonary capillary wedge; PLT = platelet count; PVR = pulmonary arteriolar resistance; RA = right atrium; SGOT = AST/aspartate aminotransferase; SGPT = ALT/alanine aminotransferase; SVR = systemic vascular resistance. In cardiopulmonary bypass, the inflow cannula was inserted in the apex of the left ventricle after removal of the apical thrombi; the outflow cannula was inserted into the ascending aorta. The Thoratec LVAD (Thoratec Laboratories Corp) was initially set at a fixed rate resulting in an output of 4.7 L/min. For mildly decreased right ventricular function, the patient was supported by low-dose dobutamine, dopamine, and milrinone infusion. An intraoperatively obtained biopsy from the left ventricular apex revealed moderate myocardial hypertrophy, areas of subendocardial and interstitial fibrosis, sparse lymphocyte-rich inflammatory infiltrates, normal vascularization of the myocardium, and absence of fresh or old myocyte necrosis. Immunohistology did not reveal any T-lymphocytes. According to these findings an active infectious myocarditis was ruled out and these histological findings together with the positive urine toxicology for cannabis were attributed to a toxic myocarditis. Postoperatively, after spending 48 hours in the intensive care unit, his liver and kidney function promptly recovered, the inotropic agents were discontinued early after the procedure, and the patient remained clinically stable under ACE-inhibitor, carvedilol, spironolactone, and low doses of furosemide. After positive testing for heparin-induced thrombocytopenia II, the anticoagulation regimen was switched to intravenous infusion of argatroban, a synthetic direct thrombin inhibitor. This therapy was monitored using the activated partial thromboplastin time and the dose was adjusted to attain the target activated partial thromboplastin time level 1.5 to 2 times the initial baseline value (not to exceed 60 seconds). Subsequently, this regimen was switched to phenprocoumon in conjunction with aspirin. Serial echocardiograms revealed a gradual unloading of the left ventricle with a gradual increase in ejection fraction. These findings remained unchanged, even during brief periods of testing during routine echocardiography with the LVAD set at a fixed rate of 40 cycles per minute. Based on these findings, and regarding the reversible nature of the underlying disease, a recovery assessment and LVAD weaning evaluation protocol was performed on postoperative day 64. The patient underwent right heart catheterization, including cardiac output measurement with the thermodilution indicator method, and transthoracal echocardiography at rest and during exercise testing with different LVAD performing modes after intravenous administration of 5,000 IU of heparin (Table 2).Table 2Weaning Evaluation ProtocolAuto Mode (baseline)Fixed Rate (baseline)Fixed Rate (baseline)Fixed Rate (25 Watt, peak exercise)Fixed Rate (50 Watt, peak exercise)Pump Frequency (L/min)7850303030Pump flow (L/min)53.21.91.91.9Heart rate (beats/min)819394133142BP (mm Hg)113/77103/73101/72116/73128/58RA (mm Hg)656910PA mean (mm Hg)1217171519PCW mean (mm Hg)714161210CI (thermodilution) (L/min/m2)2.612.662.903.203.30LVEDd (mm)4848515153LVESd (mm)3333353433LVEF (%)5353535764BP = blood pressure; CI = cardiac index; LVEDd = left ventricular end-diastolic diameter; LVEF = left ventricular ejection fraction; LVESd = left ventricular end-systolic diameter; PA = pulmonary artery; PCW = pulmonary capillary wedge; RA = right atrium. Open table in a new tab BP = blood pressure; CI = cardiac index; LVEDd = left ventricular end-diastolic diameter; LVEF = left ventricular ejection fraction; LVESd = left ventricular end-systolic diameter; PA = pulmonary artery; PCW = pulmonary capillary wedge; RA = right atrium. According to the results obtained on an ergometric bicycle with the patient in the supine position, the criteria for successful weaning was obtained, and that is, (1) the LVEF was greater than 40%, (2) the left ventricular end-diastolic diameter was less than 55 mm, and (3) the confidence interval was greater than 2.8 L/min. Consequently, we decided to plan explantation of the LVAD. During the following 4 weeks, the LVAD was set at a fixed mode, and 60 cycles per minute, whereas the serial measurement of brain natriuretic peptide and echocardiographic examinations were performed, which confirmed a constant improvement and almost complete recovery of cardiac function. Explantation was performed using cardiopulmonary bypass on day 90 post-implantation of the LVAD, which was uneventful. Before LVAD removal, intraoperative echocardiography showed hypokinesis of the septum with an ejection fraction of 50%. After LVAD removal, the ejection fraction returned to normal, and the left ventricular walls (including the septum) became hypercontractile. Hemodynamic status of the patient 48 hours after explantation (while on low dopamine doses) showed a cardiac index of 3.83 L/min/m2, blood pressure of 112/46 mm Hg, right atrial pressure of 9 mm Hg, a mean pulmonary artery pressure of 24 mm Hg, and pulmonary capillary wedge pressure of 11 mm Hg. Three weeks later the patient was discharged on enalapril (5 mg twice a day), carvedilol (3.125 mg twice a day), and spironolactone (25 mg every day). Before discharge, his echocardiogram showed an left ventricular end-diastolic diameter of 52 mm, left ventricular end-systolic diameter of 35 mm, an ejection fraction of 55%, minimal mitral and tricuspid valve regurgitation, and normal dimensions and contractility of the right ventricle. His electrocardiogram showed a sinus rhythm, a heart rate of 81 beats per minute, a normal axis, and nonspecific ST/T wave changes in leads I, aVL, V4–V6, incomplete right bundle branch block, and poor R wave progression in leads V1–V3. During a follow-up time of 7 months, the patient maintained his clinical stable condition without recurrence of heart failure symptoms. Moreover, no more excessive abuse of any drugs has been reported by his general practitioner or social workers. In this report we describe the case of a teenage boy with acute myocarditis who presented with cardiogenic shock and beginning multiorgan failure. Despite maximal medical therapy, including two inotropic agents, he had to be treated with a left Thoratec ventricular assist device (Thoratec Laboratories Corp) due to intractable heart failure symptoms and hemodynamic collapse. Ninety-six days later, the LVAD was removed after our weaning evaluation protocol had confirmed full recovery of the cardiac function. The lack of positive serology for an infectious agent, the positive cannabis testing in the urine sample, and the myocardial biopsy excluding an active myocarditis were indicative of a drug-induced (cannabis) toxic myocarditis. The deleterious effects of cocaine and other recreational drugs on the cardiovascular system are well established, but those of cannabis (marijuana) are lacking. The natural history of acute myocarditis may include spontaneous improvement, recovery, or even evolution to dilated cardiomyopathy [1D'Ambrosio A. Patti G. Manzoli A. et al.The fate of acute myocarditis between spontaneous improvement and evolution to dilated cardiomyopathy: a review.Heart. 2001; 85: 499-504Crossref PubMed Scopus (228) Google Scholar]. Toxic myocarditis is a special form of myocarditis and virtually any substance or drug (both therapeutic and industrial) can act on the myocardium and cause reversible or irreversible damage. Cannabis is one of the most widely misused recreational drugs. It has a plasma half life of 20 to 30 hours, and it can be detected in the urine of heavy users for a period of up to 2 months [2Olson K.R. Poisoning and drug overdose. 3rd ed. Appleton and Lange, Stamford, CT1999Google Scholar]. It has a dose-dependent acute effect on the autonomic nervous system with low doses producing sympathetic and high doses producing parasympathetic activation, respectively [3Ghuran A. Nolan J. Recreational drug misuse: issues for the cardiologist.Heart. 2000; 83: 627-633Crossref PubMed Scopus (150) Google Scholar]. The toxic effects of intravenously administered marijuana on the hepatic and renal function have already been described 30 years ago [4Payne R.J. Brand S.N. The toxicity of intravenously used marihuana.JAMA. 1975; 233: 351-354Crossref PubMed Scopus (16) Google Scholar], but it was only recently shown that the systemic effect of the substance is mediated by induction of increased fibrosis. According to this report, daily smoking of marijuana promotes the progression of fibrosis in patients with chronic hepatitis C and antagonism of the hepatic cannabinoid CB1 receptor can lead to inhibition of liver fibrosis [5Hezode C. Roudot-Thoraval F. Nquyen S. et al.Daily cannabis smoking as a risk factor for progression of fibrosis in chronic hepatitis C.Hepatology. 2005; 42: 63-71Crossref PubMed Scopus (253) Google Scholar, 6Teixeira-Clerc F. Julien B. Grenard P. et al.CB1 cannabinoid receptor antagonism: a new strategy for the treatment of liver fibrosis.Nat Med. 2006; 12: 671-676Crossref PubMed Scopus (453) Google Scholar]. To what extent these systemic morphologic changes can elucidate the effect of cannabis on the heart remains to be seen. Recreational drugs can cause many different cardiovascular effects ranging from harmless supraventricular arrhythmias to myocardial infarction, cardiomyopathy, and sudden cardiac death. These types of patients also tend to combine several drugs and substances, including alcohol, at the same time. These substances exert additive effects on the cardiovascular function and the long-term effects of this abuse remain uncertain. Although our patient was unwilling to provide an exact history of the drugs he used in the past he also admitted consuming “considerable amounts of alcohol when he was at parties.” His parents believed that his abuse of drugs (including alcohol) did not exceed the normal consumption of other boys in his age group. As far as we know, postoperatively, no major abuse of any drugs of our patient has been reported. Long-term drug abuse would be a contraindication for long-term mechanical circulatory support. However, for short-term support, the indication of bridge-to-recovery mechanical support should be considered a therapeutic option even after drug abuse. Levin and colleagues [7Levin H.R. Oz M.C. Chen J.M. et al.Reversal of chronic ventricular dilatation in patients with end-stage cardiomyopathy by prolonged mechanical unloading.Circulation. 1995; 91: 2717-2720Crossref PubMed Scopus (359) Google Scholar] were the first to describe the changes in pressure and volume unloading of the failing heart supported with LVAD and the shift of the end-diastolic pressure-volume relations toward near normal levels even in late stages of heart failure. These changes in hemodynamics and dimensions of the left ventricle together with the modification of the morphological, molecular, structural and neurohormonal features of the failing heart result in a partial or total functional recovery of the heart, a condition called reverse remodeling. Mechanical circulatory support with several devices has been used as a bridge-to-recovery in acute myocarditis for more than a decade [8Chen J.M. Spanier T.B. Gonzalez J.J. et al.Improved survival in patients with acute myocarditis using external pulsatile mechanical assist assistance.J Heart Lung Transplant. 1999; 18: 351-357Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar, 9Hetzer R. Alexi-Meskishvili V. Weng Y. et al.Mechanical cardiac support in the young with the Berlin Heart EXCOR pulsatile ventricular assist device: 15 years' experience.Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2006; 9: 99-108Abstract Full Text Full Text PDF Scopus (110) Google Scholar, 10Leprince P. Combes A. Bonnet N. et al.Circulatory support for fulminant myocarditis: consideration for implantation, weaning and explantation.Eur J Cardiothorac Surg. 2003; 24: 399-403Crossref PubMed Scopus (42) Google Scholar]. Yacoub recently reported the adjunctive effect of ventricular assist devices and the beta2-adrenergic-receptor agonist clenbuterol in patients with chronic, nonischemic dilated cardiomyopathy [11Birks E.J. Tansley P.D. Hardy J. et al.Left ventricular assist device and drug therapy for the reversal of heart failure.N Engl J Med. 2006; 355: 1873-1884Crossref PubMed Scopus (720) Google Scholar]. Reiss and colleagues [12Reiss N. El-Banayosy A. Arusoglu L. Blanz U. Bairaktaris A. Koerfer R. Acute fulminant myocarditis in children and adolescents: the role of mechanical circulatory assist.ASAIO J. 2006; 52: 211-214Crossref PubMed Scopus (26) Google Scholar] from our group also recently reported the successful removal of a Thoratec bi-ventricular assist device (Thoratec Laboratories Corp) in an adolescent with fulminant myocarditis after complete recovery of the left ventricular function. With our weaning protocol, we try to allow enough time for the ventricle to recover under optimized unloading conditions. Based on our clinical experience, this process requires 4 to 6 weeks and is related to each patient's individual condition and capability to exercise. We believe that this is the first case report in literature of a young teenage boy with cannabis-induced toxic myocarditis treated successfully with LVAD as a bridge-to-recovery. The LVAD was removed successfully 96 days later, after functional recovery of the heart could be demonstrated." @default.
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• W1972382107 title "Thoratec Left Ventricular Assist Device Removal After Toxic Myocarditis" @default.
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